The antiphospholipid (aPL) syndrome has been defined as the production of autoantibodies against negatively charged phospholipids or phospholipid-protein complexes, clinically associated with thrombocytopenia, thrombosis, or pregnancy loss. The syndrome is considered a disease of systemic thrombosis. The frequency of thrombosis, however, is very low, despite most patients having stable levels of circulating aPLs. Documented thrombosis occurs only in approximately 35% of the patients, and, if recurrent, the events are generally separated by years (Table 1). The most common complication, however, is disturbance of pregnancy. Patients with aPLs have an 80% to 90% pregnancy loss rate, half of which occur in the first trimester. The incidence of pregnancy loss, however, depends on the criteria upon which the patients were selected and whether pregnancy outcome is analyzed retrospectively or prospectively. In some studies the pregnancy loss rate may be as low as 50% to 75%. Even the few cases of successful pregnancy are at risk of intrauterine growth restriction (IUGR), placental abruption, prematurity, and early and severe pregnancy-induced hypertension (PIH). Therefore, the vast majority of pregnancies in the presence of aPLs result in miscarriage or are severely complicated, with indications that placental damage occurs by the first trimester. When pregnancies are evaluated in the first trimester by ultrasound, IUGR is observed commonly before the death of the fetus. The strong and relatively specific association with pregnancy complications suggests that the syndrome should be redefined as “a syndrome of pregnancy”.